Because norBNI may also act as an antagonist at mu opioid receptors (MOR) (Munro et al., 2012) and the endogenous dynorphin could bind to MOR (Raynor et al., 1994), we performed additional experiments by combining the application of norBNI with the selective MOR antagonist CTAP to further implicate the endogenous dynorphin/KOR system. Bath application of 1 μM CTAP increased IPSPs to 107 ± 5% of control, and further addition of 0.2 μM norBNI further increased IPSP amplitude to 139 ± 7% of pre-CTAP values (n = 5, Fig. 4D). Thus, norBNI was able to increase IPSPs by an additional 29 ± 6% relative to CTAP values (calculated with CTAP values being control values), suggesting that KOR mediate dynorphin effects on inhibitory transmission in CeA.
